Professor Judith Rapoport describes attempts to define cellular abnormalities in ADHD as something of a black hole, which may be due to the polygenic nature of the disorder.
It is a black hole, and I think one of the reasons is because, for the most part, the genetic advances have been with these genes like D4 or even neuregulin in schizophrenia. There are statistical associations, but statistical association means that the so-called risk gene is never present in most of the patients, and is present in loads of health people. So you don’t have the kind of a specific gene, like you have for some rare disorders, where you really can say, “Well what are the cellular effects of having Reiter’s syndrome or Fragile X or something like that?” So, there’s a couple of genes in schizophrenia that look interesting enough that you might be able to, with some of these copy number variants or some of the missense mutations from sequencing genes, you might be able to knock in those particular gene versions into animals and look at cellular effects. We are collaborating with people who will probably be doing that for the genes that we find that we have missense mutations, and so on.
The basal ganglia, a group of interconnected brain areas located deep in the cerebral cortex, have proved to be at work in learning, the formation of good and bad habits, and some psychiatric and addictive disorders.